Characterization of Right Ventricular Function After Monocrotaline-induced Pulmonary Hypertension in the Intact Rat.
From: Dept. of Cardiology, C5-P, Leiden Univ. Medical Center, PO Box 9600, 2300 RC Leiden, The Netherlands.
American journal of physiology. Heart and circulatory physiology
- Publish Date: Nov 2006
- ISSN: 0363-6135
- Volume: 291
- Issue: 5
- Pages: H2424-30
- Medium: Print
- Language: English
- Citation (JAMA): Hessel Marleen H M, Steendijk Paul, den Adel Brigit, et al. Characterization of Right Ventricular Function After Monocrotaline-induced Pulmonary Hypertension in the Intact Rat.. Am. J. Physiol. Heart Circ. Physiol. Nov 2006;291:H2424-30
Abstract
We characterized hemodynamics and systolic and diastolic right ventricular (RV) function in relation to structural changes in the rat model of monocrotaline (MCT)-induced pulmonary hypertension. Rats were treated with MCT at 30 mg/kg body wt (MCT30, n = 15) and 80 mg/kg body wt (MCT80, n = 16) to induce compensated RV hypertrophy and RV failure, respectively. Saline-treated rats served as control (Cont, n = 13). After 4 wk, a pressure-conductance catheter was introduced into the RV to assess pressure-volume relations. Subsequently, rats were killed, hearts and lungs were rapidly dissected, and RV, left ventricle (LV), and interventricular septum (IVS) were weighed and analyzed histochemically. RV-to-(LV + IVS) weight ratio was 0.29 +/- 0.05 in Cont, 0.35 +/- 0.05 in MCT30, and 0.49 +/- 0.10 in MCT80 (P < 0.001 vs. Cont and MCT30) rats, confirming MCT-induced RV hypertrophy. RV ejection fraction was 49 +/- 6% in Cont, 40 +/- 12% in MCT30 (P < 0.05 vs. Cont), and 26 +/- 6% in MCT80 (P < 0.05 vs. Cont and MCT30) rats. In MCT30 rats, cardiac output was maintained, but RV volumes and filling pressures were significantly increased compared with Cont (all P < 0.05), indicating RV remodeling. In MCT80 rats, RV systolic pressure, volumes, and peak wall stress were further increased, and cardiac output was significantly decreased (all P < 0.05). However, RV end-systolic and end-diastolic stiffness were unchanged, consistent with the absence of interstitial fibrosis. MCT-induced pressure overload was associated with a dose-dependent development of RV hypertrophy. The most pronounced response to MCT was an overload-dependent increase of RV end-systolic and end-diastolic volumes, even under nonfailing conditions.
Mesh Headings (Keywords): Animals, Blood Pressure, Cardiac Output, Hypertension, Pulmonary, Hypertrophy, Right Ventricular, Immunohistochemistry, Male, Monocrotaline, Organ Size, Rats, Rats, Wistar, Stroke Volume, Time Factors, Ventricular Dysfunction, Right, Ventricular Pressure
Check for Full Text / PubMed Unique Identifier (PMID): 16731643
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